Figure 3.

. Membrane receptor CR2 mediates IgG production in response to environmental LPS (A, B) Western blot and quantification show that on exposure to LPS stimuli, IgG levels significantly increased about one-fold, and CD46 (CD46 antigen, complement regulatory protein) blockage with the anti-CD46 antibody had no impact on the LPS-induced IgG increment. (C, D) Western blot and quantification show that FCGR1A (Fc fragment of IgG receptor Ia) blockage with anti-FCGR1A antibody had no impact on the LPS-induced IgG increment. (E-H) Western blot and quantification show that CR2 (complement receptor 2) blockage with anti-CR2 antibody brought the LPS-induced IgG increment back to the control level (E, F) CR2 blockage also brought LPS-induced p-p65 increment back to the control level (G, H). (I-L) Western blot and quantification show that on exposure to LPS stimuli, both p-p65 and IgG level significantly increased about one-fold, and the NFKB inhibitor SC75741 brought the LPS-induced p-p65 or IgG increment back to the control level. (M) Model hypothesis for A-L. LPS-induced increment of p-p65→IgG is mediated by membrane receptor CR2, not CD46 or FCGR1A. Actin was used as a loading control. Difference lower-case letters indicate significant difference between two groups.